热诱导延迟损伤大鼠心肌细胞凋亡机理的探讨  

Investigation on mechanism of hyperthermia-induced delaying of apoptosis in injured myocardial cell

作　　者：张伟华[1] 张伟才[2] 王丽娜[1] 李全凤[1] 周令望[3] 高彦辉[3] 徐长庆[1] 

机构地区：[1]哈尔滨医科大学病理生理教研室,黑龙江哈尔滨150086 [2]北京市第六医院,北京100007 [3]哈尔滨医科大学克山病研究所,黑龙江哈尔滨150086

出　　处：《中国地方病学杂志》2003年第4期292-294,共3页Chinese Jouranl of Endemiology

摘　　要：目的　探讨热诱导延迟过氧化氢 (H2 O2 )造成大鼠心肌细胞凋亡机理。方法　体外培养大鼠乳鼠心肌细胞同时温度诱导细胞产生热休克蛋白 70 (HSP70 ) ,用 H2 O2 造成心肌细胞损伤。采用 Western Blotting、流式细胞仪、Bcl-2原位杂交、免疫组化检测 Caspase-3等作为检测指标 ,观察心肌细胞损伤 ,以及 HSP70 对心肌细胞的保护作用。结果　温度诱导后 HSP70 在胞浆中大量表达 ,保护组凋亡率显著低于损伤组 ,Bcl-2和 Caspase-3在损伤组大量表达。结论　 HSP70 可延迟细胞凋亡 。Objective To investigate the relationship bet ween heat and injured myocardial cell by H 2O 2 in rats.Methods Myocardial cell was cultured in vitro.HSP 70 was induced by hyperthermia. H 2O 2 was used to injure myocardial cells of different groups.Western Blotting,flow cytometry,Bcl-2 in situ hybridization an d Caspase-3 immunohistochemistry were employed to observe the myocardial cell o f different groups.Results The up-regulation of HSP 70 was demonstra ted by Western Blotting.The apoptosis rate was significantly lower in the protec tive group than in the injured group.Bcl-2 and Caspase-3 were expressed obviou sly in injured group.Conclusions HSP 70 can delay apoptosis and protect myocardial cell.

关 键 词：热诱导 大鼠 心肌细胞 细胞凋亡 热休克蛋白70 HSP70 过氧化氢 H2O2 

分 类 号：R541[医药卫生—心血管疾病]